| 一氧乙酰旋覆花内酯对血管紧张素Ⅱ诱导的肥大心肌细胞的保护性作用 |
| 投稿时间：2017-07-26 修订日期：2017-09-12 点此下载全文 |
| 引用本文：酉鹏华,何晓敏,林静,陈海潮,崔倩卫.一氧乙酰旋覆花内酯对血管紧张素Ⅱ诱导的肥大心肌细胞的保护性作用[J].医学研究杂志,2018,47(4):134-138 |
| DOI：
10.11969/j.issn.1673-548X.2018.04.033 |
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| 中文摘要:目的 探讨ABL在心肌细胞肥大中的作用及其机制。方法 体外培养H9C2心肌细胞，血管紧张素Ⅱ（AngⅡ）构建心肌细胞肥大模型；模型组给予1μmol/L AngⅡ刺激24h、ABL处理组给予AngⅡ刺激，同时给予5μmol/L和10μmol/L ABL处理24h。采用心肌细胞肌动蛋白α-actinin染色评价心肌细胞大小，采用RT-PCR检测肥厚相关基因心房利钠肽（ANP）、脑钠肽（BNP）、肌球蛋白重链β（β-MHC）的表达；蛋白印迹（Western blot）法检测信号通路蛋白的表达。结果 与模型组比较，5μmol/L和10μmol/L ABL处理组心肌细胞面积明显降低（P<0.05）；ANP、BNP、β-MHC肥厚相关基因表达降低（P<0.05），且其抗心肌细胞肥大呈现剂量依赖性（P<0.05）。Western blot法检测结果显示ABL处理组AMPKa磷酸化水平增高（P<0.05），而Akt、mTOR、GSK3β的磷酸化明显抑制（P<0.05）；AMPKa拮抗剂Compound C可阻断ABL的心肌保护作用。结论 ABL可通过激活AMPKa信号通路，调节Akt/Mtor/GSK3β对AngⅡ诱导的心肌细胞肥大发挥保护性作用。 |
| 中文关键词:一氧乙酰旋覆花内酯 心肌细胞 血管紧张素Ⅱ AMPKa Akt |
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| Protective Effect of 1-O-acetylbritannilactone in Angiotensin II Induced Cardiomyocyte Hypertrophy |
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| Abstract:Objective To explore the role of ABL in cardiomyocytes hypertrophy. Methods H9C2 myocardial cells were stimulated with Angiotensin Ⅱ (AngⅡ). The cell surface area was measured by α-actinin staining. The mRNA expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and myosin heavy chain beta (β-MHC) was measured by RT-PCR. The protein expression of AMPKa signaling proteins were detected by Western blot. Results Compared with model group, cell surface area in 5μmol/L and 10μmol/L ABL treatment group was decreased significantly. The expression of ANP, BNP, β-MHC was decreased in a dose dependent manner. The phosphorylation of AMPKa expression was decreased in model group. After treatment with ABL, the levels of phosphorylation of AMPKa was up-regulated, and phosphorylation of Akt, mTOR, GSK3β was significantly decreased. AMPKa inhibitor compound C abolished the protective effect of ABL. Conclusion ABL can protect cardiomyocytes against AngⅡ induced cardiomyocytes hypertrophy by regulating AMPKa/Akt/mTOR/GSK3β signal pathway. |
| keywords:1-O-acetylbritannilactone Cardiomyocytes AngⅡ AMPKa Akt |
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